HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) An erratum has been published Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Visvanathan, S. Articles by McNeil, H. P. Search for Related Content PubMed PubMed Citation Articles by Visvanathan, S. Articles by McNeil, H. P.

Monocyte Tissue Factor Induction by Activation of ß₂-Glycoprotein-I-Specific T Lymphocytes Is Associated with Thrombosis and Fetal Loss in Patients with Antiphospholipid Antibodies¹

Sudha Visvanathan^*, Carolyn L. Geczy, Jason A. Harmer and H. Patrick McNeil^2,*,

^* Inflammation and Cytokine Research Units, School of Pathology, University of New South Wales, Sydney, Australia; and Department of Rheumatology, Prince of Wales Hospital, Sydney, Australia

Antiphospholipid (aPL) syndrome (APS) is characterized by thromboembolic events, thrombocytopenia, or recurrent miscarriage associated with aPL Abs with specificity for ß₂-glycoprotein-I (ß2GPI). We recently reported that at least 44% of patients with the APS possess circulating type 1 (Th1) CD4⁺ T cells that proliferate and secrete IFN- when stimulated with ß2GPI in vitro. In this study, we show that stimulation of PBMCs from 20 APS patients with ß2GPI induced substantial monocyte tissue factor (TF) (80 ± 11 TF stimulation index (TF-SI)), whereas no induction was observed using PBMCs from 13 patients with aPL Abs without APS (6 ± 1 TF-SI) or 7 normal and 7 autoimmune controls (5 ± 1 and 3 ± 1 TF-SI, respectively) (p < 0.0001). TF induction on monocytes by ß2GPI was dose dependent and required CD4⁺ T lymphocytes and class II MHC molecules. Because monocyte TF induction by ß2GPI was observed in all patients with APS, but not in any patient with aPL Abs without APS, this response is a potentially useful predictor for APS in patients with aPL Abs, as well as providing mechanistic insight into thrombosis and fetal loss in these patients.

This article has been cited by other articles:

				M. van Lummel, M. T. T. Pennings, R. H. W. M. Derksen, R. T. Urbanus, B. C. H. Lutters, N. Kaldenhoven, and P. G. de Groot The Binding Site in {beta}2-Glycoprotein I for ApoER2' on Platelets Is Located in Domain V J. Biol. Chem., November 4, 2005; 280(44): 36729 - 36736. [Abstract] [Full Text] [PDF]

				J. George, N. Yacov, E. Breitbart, L. Bangio, A. Shaish, B. Gilburd, Y. Shoenfeld, and D. Harats Suppression of early atherosclerosis in LDL-receptor deficient mice by oral tolerance with {beta}2-glycoprotein I Cardiovasc Res, June 1, 2004; 62(3): 603 - 609. [Abstract] [Full Text] [PDF]

				T. E. Warkentin, W. C. Aird, and J. H. Rand Platelet-Endothelial Interactions: Sepsis, HIT, and Antiphospholipid Syndrome Hematology, January 1, 2003; 2003(1): 497 - 519. [Abstract] [Full Text] [PDF]

				J. H. Rand Molecular Pathogenesis of the Antiphospholipid Syndrome Circ. Res., January 11, 2002; 90(1): 29 - 37. [Abstract] [Full Text] [PDF]

				T. Arai, K. Yoshida, J. Kaburaki, H. Inoko, Y. Ikeda, Y. Kawakami, and M. Kuwana Autoreactive CD4+ T-cell clones to {beta}2-glycoprotein I in patients with antiphospholipid syndrome: preferential recognition of the major phospholipid-binding site Blood, September 15, 2001; 98(6): 1889 - 1896. [Abstract] [Full Text] [PDF]